Poster #92 - Associations between Family Environment and Brain Function and Structure are Mediated by Accelerated Pubertal Development

• In Event: 1-115 - Poster Session 03
  In Poster Session: PS 03 Section - Family Context & Processes

Integrative Statement

Psychosocial Acceleration Theory suggests that pubertal maturation is accelerated in response to adversity (Belsky, Steinberg, & Draper, 1991). Evidence suggests that development of the amygdala-medial prefrontal cortex (mPFC) circuit—involved in emotion regulation—is accelerated following suboptimal care (Gee et al., 2013; Thijssen et al., 2017). It is unclear if these findings are related. Here, we assess whether associations between a child’s family environment and the amygdala-mPFC circuit are mediated by pubertal development in 9-to 10-year old children.
This study includes 2000+ participants from the Adolescent Brain Cognitive Development Study, a multi-site prospective population-based United States cohort (http://dx.doi.org/10.15154/1412097). Using Structural Equation Modeling, three latent variables describing demographic and parent information (e.g. socioeconomic status, parental relationship status), child reported data on parenting and family dynamics (e.g. parental acceptance, family conflict), and parent reported data on family dynamics (e.g. parent-child conflict), were compiled into a higher-level Family Environment latent variable (RMSEA = 0.04). To test predictive validity, the Family Environment latent variable was related to Child Behavior Checklist Eternalizing and Internalizing Broadband Scales (r = -.38, r = -.23, respectively), as well as to the Strength and Difficulties Questionnaire Prosocial scale (r = .18, r = .21, for parent and child reported scores, respectively). Image processing and analysis were performed by the ABCD consortium. Cingulo-opercular network (CON)-amygdala resting-state functional connectivity (FC), amygdala volume, anterior cingulate cortex (ACC) thickness (CT) and area (CA), and fractional anisotropy (FA) were used to represent the amygdala-mPFC circuit. Mediation models were performed in MPLUS and controlled for age, race, sex, site, and total brain volume. For amygdala volume and ACC CA, quadratic mediation was tested using the SPSS Medcurve macro (Hayes and Preacher, 2010). To explore sex differences, sex stratified mediation analyses were performed.
For left CON-Amygdala FC, ACC CT, and ACC FA, significant indirect effects were found (B = 0.01, p = .012; B = -0.014, p = .007; B = -0.013, p = .015, respectively). For right CON-Amygdala FC, a significant total (B = 0.04, p = .041), but no significant (in)direct effects were found (B = 0.01, B = 0.04, for indirect and direct, respectively). For ACC CA, there was a quadratic relation between pubertal stage and ACC FA (b = -0.144, p = .003) and an instantaneous indirect effect for +1 SD of the Family Environment score (b = -0.01). For effect estimates of the sex stratified analyses, see Figure 2. For both boys and girls, family environment was related to pubertal stage (B = -.156 to -.211, B = -.108 to -.185, respectively). For girls, but not for boys, however, significant associations between pubertal stage and proxies of the amygdala-mPFC circuit were found, suggesting mediation of the association between family environment and the amygdala-mPFC circuit for girls only.
Despite small effect sizes, these findings indicate that structural and functional connectivity of circuits important for emotional behavior are distinct in the context of adverse family environments and are associated with accelerated pubertal development.

Authors

• Sandra Thijssen, Erasmus University Rotterdam
  Presenting Author

• Paul Collins, University of Minnesota
  Non-Presenting Author

• Monica Luciana, University of Minnesota
  Non-Presenting Author